Magnesium research最新文献

The hematopoietic U937 cells are able to differentiate into monocytes, macrophages, or osteoclasts when stimulated, respectively, with vitamin D3 (VD3), phorbol 12-myristate 13-acetate (PMA) or PMA plus VD3. We have previously demonstrated that magnesium (Mg) strongly potentiates the osteoclastic differentiation of U937 cells. In this study, we investigated whether such an effect may be ascribed to a capacity of Mg to modulate the monocyte differentiation of U937 cells and/or to an ability of Mg and VD3 to act directly and independently on the early phases of the osteoclastic differentiation. To address this issue, we subjected U937 cells to an individual and combined treatment with Mg and VD3 and then we analyzed, by flow cytometry and quantitative real-time polymerase chain reaction, the expression of a number of genes related to the early phases of the differentiation pathways under consideration. The results obtained indicated that Mg favors the monocyte differentiation of U937 cells induced by VD3 and at the same time, Mg contrasts the inhibitory effect that VD3 exerts on the osteoclastic differentiation in the absence of PMA. The crucial and articulated role played by Mg in diverse pathways of the osteoclastic differentiation of U973 cells is emphasized.

Chronic stress has been implicated in the development and progression of heart disease. In the past decade, a link between chronic stress and cardiac fibrosis has been described. Here, we focused on investigating the effects of one of the key molecular effectors of the stress response-adrenocorticotropic hormone (ACTH) on cardiac histopathology. More importantly, as the literature data support interplay between magnesium (Mg) and the hypothalamo-pituitary-adrenal (HPA) stress system, we explored potential cardioprotective effects of Mg supplementation in a rat model of ACTH-induced cardiac remodeling. Protracted ACTH exposure in rats resulted in a prominent increase in proliferation of fibroblasts and excessive collagen deposition in the heart, accompanied by enhanced proliferation of cardiomyocytes and vascular endothelial cells. Our results show, for the first time, that administration of Mg in rats was effective in ameliorating the development of ACTH-evoked cardiac fibrosis, while facilitating cardiomyocyte proliferation. Furthermore, we propose that Mg supplementation attenuates ACTH-induced HPA axis hyperactivity, as one of the underlying plausible mechanisms, which may contribute to its cardioprotective effects.

Modern life and the Western industrial diet has enhanced the reduction of magnesium in our food, which may contribute to a marginal or absolute magnesium deficiency. Magnesium deficiency is evident in, among others, the elderly population, those after myocardial infarction and/or chronic heart failure, and diabetics. In Israel, over 60% of the drinking water originates from desalinated seawater lacking magnesium, which may cause hypomagnesemia. Magnesium deficiency can easily be treated by magnesium supplementation if we are aware of the situation. This paper summarizes the magnesium chapter in a position paper published in April 2021 by the Israeli Cardiology Society together with the Israeli Dietetic Association. It summarizes evidence-based nutritional recommendations for prevention and treatment of cardiovascular disease, with emphasis on the level of evidence and practical recommendations according to the European Society of Cardiology definitions. The best recommendation is to increase consumption of magnesium-rich food, such as leafy green vegetables (mainly spinach), nuts, avocado, whole grains, legumes (e.g., beans, peas and soy beans), chocolate and certain seafood. However, for people who do not get sufficient magnesium from their diet completing the daily amount, as needed, with supplements of up to 600 mg/day should be considered. In addition, serum magnesium levels should be checked at least every six months in patients with heart failure, people taking diuretic therapy, and people taking proton-pump inhibitors. In addition, it may be beneficial to add magnesium following myocardial infarction in people with hypertension and in heart failure patients in order to reduce cardiovascular morbidity and mortality (class of recommendation IIa, level of evidence B).

The objective of the present research is to develop and optimize a chewable tablet containing synergistic combination of magnesium orotate dihydrate (MOD), cholecalciferol (CHOL) and menaquinone-7 (MK-7) as per product development guidelines of ICH Q8 (R2). The effects of critical variables on quality attributes of chewable tablets were evaluated using 30 runs based design of experiment (DoE) after risk assessment. Optimized formulation was found to be the one that was prepared with moderate granulation time of 7.23 min and contained 14 mg/tablet binder, 31 mg/tablet disintegrant and 11.377 mg/tablet lubricant. Prepared tablets were evaluated for prescribed pharmacopoeial and regulatory quality checks. Optimized formulation was found to have very low disintegration time of 6.06 min and 87.39% dissolution of MOD within 15 min in acidic media (0.1 N HCl), which ensure that the developed formulation behaves as a solution following oral administration. Stability studies under accelerated conditions revealed that the developed formulation can retain its quality characteristics throughout its shelf life. Pharmacokinetics study of chewable tablets in male Wistar rats shows that the time to reach maximum plasma or serum concentration (T_max) was 3 h for MOD and 6 h for both CHOL and MK-7. Maximum plasma or serum concentration (C_max) of MOD, CHOL and MK-7 was found to be 7.233 ± 1.159, 8.182 ± 0.783 and 8.331 ± 0.863 μg/mL [mean ± standard deviation (SD)], respectively. The area under the curve (AUC ₀-_t) for MOD, CHOL and MK-7 was 80.692 ± 11.197, 124.325 ± 17.101 and 126.568 ± 12.064 μg.mL.h^-1 (mean ± SD), respectively. Comparison of pharmacokinetic data of chewable tablets with a mixture of pure drugs proves that the developed formulation can efficiently deliver all the three nutrients in blood and is capable to elicit desired pharmacological response.

This study aimed to determine the relationship between hospital-acquired dysmagnesemia and in-hospital mortality in critically ill patients. A retrospective cohort study was conducted on critically ill patients who had normal serum magnesium levels on admission. Data were extracted from the Multiparameter Intelligent Monitoring in Intensive Care III database. The normal range of serum magnesium was 1.6-2.6 mg/dL. In-hospital serum magnesium levels were categorized based on the occurrence of hospital-acquired hypomagnesemia and hypermagnesemia. Hospital-acquired hypomagnesemia and hypermagnesemia in the same patient were defined as a patient with the lowest level of serum magnesium of <1.6 mg/dL and the highest level of serum magnesium of >2.6 mg/dL, respectively. The in-hospital outcomes were collected. The findings revealed that 27.2% of patients developed hospital-acquired dysmagnesemia. In-hospital mortalities were 8.8% in patients with persistently normal serum magnesium levels, 12.2% in patients with hospital-acquired hypomagnesemia only, 18.4% in patients with hospital-acquired hypermagnesemia only, and 20.6% in patients with both hospital-acquired hypomagnesemia and hypermagnesemia. Compared to patients with persistently normal serum magnesium in hospital, those with hospital-acquired hypermagnesemia only [odds ratio (OR) = 1.346, P < 0.001] and those with both hospital-acquired hypomagnesemia and hypermagnesemia (OR = 1.333, P = 0.001) were significantly associated with higher in-hospital mortality. Hospital-acquired dysmagnesemia was common among critically ill patients. Hospital-acquired dysmagnesemia, especially hospital-acquired hypermagnesemia, was significantly associated with increased in-hospital mortality in critically ill patients.

The objective of this study was to investigate the effects of a novel form of biotin (magnesium biotinate) on serum glucose, lipid profile, and hepatic lipid metabolism-related protein levels in rats. Forty-two rats were divided into six groups and fed a standard diet-based egg white powdered diet supplemented with either d-biotin at 0.01, 1, or 100 mg/kg BW or magnesium biotinate at 0.01, 1, or 100 mg/kg BW for 35 days. Neither form of biotin influenced (p > 0.05) serum glucose or insulin concentrations. Serum total cholesterol and triglyceride decreased with biotin from both sources (p < 0.05). Concentrations were lower with magnesium biotinate when comparing the 1 mg/kg dose (p < 0.05). Serum, liver, and brain biotin and liver cyclic guanosine monophosphate (cGMP) concentrations were greater when rats were treated with magnesium biotinate versus d-biotin, particularly when comparing the 1 and 100 mg/kg dose groups (p < 0.05). Both biotin forms decreased the liver SREBP-1c and FAS and increased AMPK-α1, ACC-1, ACC-2, PCC, and MCC levels (p < 0.05). The magnitudes of responses were more emphasized with magnesium biotinate. Magnesium biotinate, compared with a commercial d-biotin, is more effective in reducing serum lipid concentrations and regulating protein levels of lipid metabolism-related biomarkers.

Magnesium (Mg) is critically involved in the pathophysiology of multiple human diseases; nevertheless, Mg disorders are often poorly considered in the clinical practice. To update the prevalence and incidence of hypomagnesemia and hypermagnesemia in a real-life scenario, which better represents clinical practice, we analyzed data from 12,696 patients whose Mg serum levels were measured from January 1, 2015, through December 31, 2017 at our University Hospital. Hypomagnesemia and hypermagnesemia were defined by Mg concentrations <1.5 mg/dL (0.6 mmol/L) and >3.8 mg/dL (1.5 mmol/L), in accordance with the reference values for magnesemia of our laboratory (1.5-3.8 mg/dL). The prevalence of hypomagnesemia and hypermagnesemia was 8.43% (n=1071) and 1.78% (n=226), respectively. Hypomagnesemia occurred more frequently in females compared with males [53.3% (n=560) versus 47.7% (n=511), χ²=4.03, p<0.045]; the highest prevalence of hypomagnesemia was found in patients over 65 yr. [59.01% (n=632)], when compared with the other age groups [59.01% (n=632) versus 9.52% (n=102) in patients aged 0-18 yr. and 31.46% (n=337) in patients between 19 and 65 yr., χ²=592.64; p<0.0001)]. Incidence of hypomagnesemia decreased over time in subjects over 65 yr. (r=-0.99; p=0.07). Geriatrics, oncology, and intensive care division showed the highest incidences of hypomagnesemia. Mg disorders and remarkably hypomagnesemia are quite common in the clinical practice, particularly in older hospitalized patients. Thus, they should be routinely checked and corrected.